Curcumin exerts a protective effect against premature ovarian failure in mice

Abstract

This study was designed to investigate the protective effect of curcumin against d-galactose (d-gal)-induced premature ovarian failure (POF) in mice. A mouse POF model was induced by subcutaneous injection of d-gal (200 mg/kg/day) daily for 42 days. Mice in the curcumin group received both d-gal treatment and intraperitoneal injection of curcumin (100 mg/kg/day) for 42 days. Ovarian function, oxidative stress and apoptosis were evaluated. The P, E2 and SOD levels were higher, and the FSH, LH and MDA levels were significantly lower in the curcumin group than those in the d-gal group. The proportion of primordial follicles was also significantly higher in the curcumin group than that in the d-gal group. In addition, curcumin treatment after d-gal administration resulted in significantly lower Sod2, Cat, 8-OhdG, 4-HNE, NTY and senescence-associated protein P16 expression levels, higher Amh expression levels and less apoptosis in granulosa cells than was observed in the d-gal group. Moreover, the p-Akt, Nrf2 and HO-1 protein expression levels were significantly higher and the apoptosis-related cleaved caspase-3 and -9 protein expression levels were markedly lower in the curcumin group than in the d-gal group. In conclusion, curcumin effectively inhibited d-gal-induced oxidative stress, apoptosis and ovarian injury via a mechanism involving the Nrf2/HO-1 and PI3K/Akt signaling pathways, suggesting that curcumin is a potential protective agent against POF.

Catalpol protects rat ovarian granulosa cells against oxidative stress and apoptosis through modulating the PI3K/Akt/mTOR signaling pathway

“…It is well known that the PI3K/Akt signaling pathway plays a crucial role in the regulation of GCs growth apoptosis during follicular development [25,26]. Emerging evidence has proven activation of PI3K/Akt signaling pathway protects GCs from oxidative stress and apoptosis [27][28][29]. Interestingly, previous study has reported that catalpol promotes axonal growth via regulating miR-124 to activate PI3K/Akt/mTOR pathway in neurons after ischemia [30].…”

Establishment of a Mouse Model of Premature Ovarian Failure Using Consecutive Superovulation

“…Western blotting analysis was performed according to previously described methods [12]. Briefly, 50 μg of total lysate obtained from ovarian tissue was subjected to 15% polyacrylamide gel electrophoresis and then transferred to a cellulose acetate membrane.…”

“…Currently, mouse models of female reproductive aging are divided into two categories: genetic mutation animal models, such as the follitropin receptor knockout animal model [4, 5] and the dioxin/aryl hydrocarbon receptor knockout animal model [6, 7]; and poison damage models, such as the 4-vinylcyclohexene diepoxide-induced female reproductive aging model [8, 9] and the D-galactose-induced female reproductive aging model [10-12]. Although these animal models show an increase in follicular consumption or even depletion, the resulting estrous cycle disorders, decreased sex hormone secretion and decrease in or loss of fertility may indicate one or more pathological states and thus do not simulate the real pathophysiological condition of ovarian aging [8, 13].…”

Investigation of the Relation between Follicular Atresia and Granulosa Cells in Terms of Cell Death Mechanisms in Premature Ovarian Failure Model

“…Loss of GCs with FA leads to premature depletion of ovarian reserves and POF formation. According to literature POF animal model is established with CTX [1][2][3]. The two most well-known cell death types in the FA process are apoptosis and autophagy.…”

“…The two most well-known cell death types in the FA process are apoptosis and autophagy. In addition, recently it has been suggested that paraptosis, which is a type of cell death has associated with ERS has been played a role in this process [1,4]. In this study, it was aimed to establish the POF model in C57BL/6 female mice that was induced by CTX and evaluation of apoptosis, autophagy and paraptosis via indirect IHC method in order to determine the CDM that play a role in FA process.…”